Hypoglycemia pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Pathogenesis of hypoglycemia depends on failure of physiological defense mechanisms and hormones such as insulin, glucagon | Pathogenesis of hypoglycemia depends on failure of physiological defense mechanisms and hormones such as insulin, glucagon an epinephrine. This leads to low glucose level that affect primarily the brain causing nervous symtptoms. | ||
==Pathogenesis== | ==Pathogenesis== | ||
Pathogenesis of hypoglycemia depends on failure of physiological defense mechanisms to correct hypoglycemia. Most of these defensive | Pathogenesis of hypoglycemia depends on failure of physiological defense mechanisms to correct hypoglycemia. Most of these defensive | ||
Revision as of 18:40, 17 July 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Mohammed Abdelwahed M.D[2]
Overview
Pathogenesis of hypoglycemia depends on failure of physiological defense mechanisms and hormones such as insulin, glucagon an epinephrine. This leads to low glucose level that affect primarily the brain causing nervous symtptoms.
Pathogenesis
Pathogenesis of hypoglycemia depends on failure of physiological defense mechanisms to correct hypoglycemia. Most of these defensive are hormones control glycogenolysis and gluconeogenesis:
- Insulin
The most important mechanism to counterregulate hypoglycemia is the ability to suppress insulin release. This can't occur in patients with absolute beta-cell failure those with type 1 diabetes and long-standing type 2 diabetes.[1]High insulin inhibits hepatic glycogenlysis
causing more hypoglycemia.
- Glucagon
Hypoglycemia stimulates secretion of glucagon which is the main counteregulatory hormone. This may be the result of beta-cell failure and high insulin that inhibits glucagon secretion.[2]
- Epinephrine
Epinephrine response to hypoglycemia also becomes attenuated in many patients.[3]
An attenuated epinephrine response causes defective glucose counterregulation and hypoglycemia unawareness.[4] This may be due to shifting the glycemic threshold for the sympathoadrenal response to a lower plasma glucose concentration.
brain is dependent on a continual supply of glucose diffusing from the blood into the interstitial tissue within the central nervous system and into the neurons themselves.
If the amount of glucose supplied by the blood falls, the brain is one of the first organs affected. Impairment of action and judgement, Seizures may occur as the glucose falls further, resulting in coma. These brain effects are collectively referred to as neuroglycopenia. This can include impairment of cognitive function, motor control, or even consciousness.
References
- ↑ Dunning BE, Gerich JE (2007). "The role of alpha-cell dysregulation in fasting and postprandial hyperglycemia in type 2 diabetes and therapeutic implications". Endocr Rev. 28 (3): 253–83. doi:10.1210/er.2006-0026. PMID 17409288.
- ↑ Raju B, Cryer PE (2005). "Loss of the decrement in intraislet insulin plausibly explains loss of the glucagon response to hypoglycemia in insulin-deficient diabetes: documentation of the intraislet insulin hypothesis in humans". Diabetes. 54 (3): 757–64. PMID 15734853.
- ↑ Dagogo-Jack SE, Craft S, Cryer PE (1993). "Hypoglycemia-associated autonomic failure in insulin-dependent diabetes mellitus. Recent antecedent hypoglycemia reduces autonomic responses to, symptoms of, and defense against subsequent hypoglycemia". J Clin Invest. 91 (3): 819–28. doi:10.1172/JCI116302. PMC 288033. PMID 8450063.
- ↑ Geddes J, Schopman JE, Zammitt NN, Frier BM (2008). "Prevalence of impaired awareness of hypoglycaemia in adults with Type 1 diabetes". Diabet Med. 25 (4): 501–4. doi:10.1111/j.1464-5491.2008.02413.x. PMID 18387080.